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Physiology > Bone Physiology > Flashcards

Bone Physiology Flashcards

1
Q

Protein in the bone matrix is >90%

A

Collagen

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2
Q

Most abundant cells found in the compact bone are the

A

Osteocytes

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3
Q

An osteoblast becomes an osteocyte when it

A

Gets trapped in the bone matrix it has secreted

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4
Q

Two varieties of bone:

A
  1. Compact2. Trabecular
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5
Q

Common site of bone growth, particularly long bones

A

Epiphysial Plate

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6
Q

Three processes that halt bone growth

A
  1. Epiphyses unite with shaft (epiphysial closure)2. Cartilage cells stop proliferating3. VEGF secreted -> vascularization/ ossification
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7
Q

Three most important hormone regulators of Calcium in the blood

A

Parathyroid Hormone (PTH), Vitamin D, calcitonin

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8
Q

Transcription Factor associated with osteoblast precursor cells

A

RUNX 2

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9
Q

In mice, knocking out RUNX2 led to

A

Non-ossification of bones (osteoblasts not maturing) -> floppy mice!

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10
Q

Products and enzymes that identify an osteoblast as active

A

Collagen, Alkaline phosphatase, osteoprotegerin (OPG), RANK ligand

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11
Q

These 2 factors from osteoblasts stimulate maturation of an active osteoclast

A

RANK LIGAND and OPG

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12
Q

“Decoy” OPG can bind ________ to inhibit osteoclast differentiation

A

RANK Ligand

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13
Q

In osteoporosis, estrogen replacement therapy will upregulate _____ to inhibit osteoclast activity

A

OPG

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14
Q

Full bone replacement occurs, on average, every

A

10 years

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15
Q

Most of the bodys calcium is in (body part)

A

Bone (98%)

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16
Q

Physiologic roles of Calcium

A
  1. Bone formation
  2. Neuronal excitability
  3. NT release
  4. Muscle contraction
  5. Membrane integrity
  6. Blood Coagulation
17
Q

Hypocalcemia can lead to:

A
  1. Tetany (increased permeability of neurons to Na+, more action potentials, muscle spasm)
  2. Parasthesias (things feel funny)
  3. Muscle cramps
  4. Convulsions
  5. Laryngospasms
18
Q

Hypercalcemia leads to:

A

Anorexia, Nausea, (GI symptoms basically), lethargy, coma

19
Q

In most cases Calcium and Phosphate are co-regulated, except in

A

the kidney

(they are regulated in opposite directions)

20
Q

Causes of hypercalcemia

A

Hyperparathyroidism

Cancer

21
Q

Causes of hypocalcemia

A

Hypoparathyroidism

Vitamin D Deficiency

Chronic Kidney disease (cant reabsorb in tubules)

Calcium malabsorption

22
Q

How does Vitamin D moderate calcium

A

Pulls in Ca2+ from gut

23
Q

Mechanism of Phosphorous entrance/exit from body (what mediates)

A

Phosphorous pulled in from gut w/ help from transporter upregulated by Vitamin D

Filtered in glomerulus, most reabsorbed.

PTH can inhibit resorption transporter (block P, leaves via urine)

24
Q

Causes of hypophosphatemia

A

Inadequate P absorption (gut disorder or Vitamin D deficiency)

Excessive renal excretion (renal disease/renal failure)

Hyperparathyroidism (too much PTH made, leads to blockage of resabsorption at kidney -> pee too much out)

25
Q

Phosphorous necessary for:

A

energy (ATP), active enzymes and proteins

26
Q

Causes of hyperphosphatemia

A

Impaired glomerular filtration (cant get P out of blood)

Hypoparathyroidism (PTH not present, too much resorption of P at tubule)

27
Q

What is PTHrP and what does it do?

A

Protein associated with PTH, binds to the same receptor, though they are usually found in separate places

Produced as a “paracrine” hormone in tissues local to the receptor.

A kind of developmental hormone

  • Stimulates cartilage cells to proliferate and maintain proliferative state (used both in utero bone formation and after birth)
  • In brain, PTHrP inhibits excitotoxic damage to developing neurons
  • Critical to teeth eruption
28
Q

In normal circumstances, what is the body’s response to low serum calcium?

A

Parathyroid glands produce more parathyroid hormone, which increases calcium reabsorption in the kidneys.

Increase in Vitamin D formation (via liver and kidney) that will “pull in” more calcium from gut.

Possible to get bone resorption, but much less common in non-pathogenic people

29
Q

1,25 OHD (Vitamin D) binds to transcalciferin [TC] and then acts on which part of the cell

A

In the Nucleus, binds to the RXR (retanoic acid receptor), which turns off repressors, recruits activators, and turns on the needed genes to get calcium into the blood

30
Q

Vitamin D increases _ _, _ _, and _ _ to increase absorption of Calcium from gut and increases expression of enzymes to increase Ca retention at kidney

A

Calbindins, Ca ATPases, TRPV6 (transporter across lumen)

31
Q

Why would inactive Vitamin D be made?

A

Plasma calcium too high. As it is being processed, vitamin D shunted towards inactive form until balanced

32
Q

Where is calcitonin made?

A

Parafollicular Cells in the Thyroid

33
Q

What does calcitonin do, broadly?

A

Decreases bone breakdown

Increases excretion of calcium from kidney

Ultimately wants to reduce serum calcium

34
Q

What does calcitonin block?

A

Blocks osteoclasts from breaking down bone (and thus releasing calcium into blood).

35
Q

What is the effect of estrogen on osteoclasts?

A

estrogen inhibits secretion of interleukins/ enzymes (IL-1, IL-6, TNF alpha) associated with development of osteoclasts

Upregulates OPG to bind RANK ligand and inhibit osteoclast development

Stimulates production of TNF beta that causes osteoclast apoptosis

36
Q

Disorders of bone mineral homeostasis (4)

A

Osteoporosis- overactive osteoclasts due to low estrogen)

Osteomalacia (or ricketts)- inadequate mineralization of bones due to Vitamin D deficiency

Osteopetrosis- unopposed osteoblasts (osteoclasts not breaking down, leads to “rock bones”)

Pagets Disease- osteoclasts work abnormally in weird places, leads to abnormal bone remodeling (weird faces)

Physiology (10 decks)

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